作者: Ramya Rajagopalan , Lee Kroos
DOI: 10.1128/JB.00788-16
关键词:
摘要: Myxococcus xanthus undergoes multicellular development when starved. Thousands of rod-shaped cells coordinate their movements and aggregate into mounds in which differentiate spores. Mutations the dev operon impair development. The encompasses a clustered regularly interspaced short palindromic repeat-associated (CRISPR-Cas) system. Null mutations devI, small gene at beginning operon, suppress developmental defects caused by null downstream devR devS genes but failed to in-frame deletion devT We provide evidence that original mutant has second-site mutation. show mutants exhibit indistinguishable from mutants, mutation devI suppresses similarity DevTRS proteins components CRISPR-associated complex for antiviral defense (Cascade), together with our molecular characterization support model form Cascade-like subcomplex negatively autoregulates transcript accumulation prevents DevI overproduction would strongly inhibit sporulation. Our results also suggest transiently inhibits sporulation regulated normally. mechanism transient inhibition may involve MrpC, key transcription factor, whose translation appears be weakly inhibited DevI. Finally, indicates very little exo is required sporulation, surprising since Exo help polysaccharide spore coat.IMPORTANCE CRISPR-Cas systems typically function as adaptive immune bacteria. system M. been proposed prevent bacteriophage infection during development, how controls elusive. Recent supported DevR DevS DevI, predicted 40-residue inhibitor genetic DevT functions overproduction. spores about 6 h earlier lacking than wild type. Only minority natural isolates appear have functional promoter suggesting evolved recently niches where delayed and/or protection proved advantageous.